Contrasting antioxidant and cytotoxic effects of peroxiredoxin I and II inPC12 and NIH3T3 cells

We examined the impact of peroxiredoxin-I (Prx-I) and peroxiredoxin-II (Prx -II) stable transduction on oxidative stress in PC12 neurons and NIH3T3 fib roblasts and found variability depending on cell type and Prx subtype. In P C12 neurons, Prx-II suppressed reactive oxygen species (ROS) generation by 36% (p < 0.01) relative to vector-infected control cells. However. in NIH3T 3 fibroblasts, Prx-II overexpression resulted in a 97% (p < 0.01) increase in ROS generation. Prx-I transduction elevated ROS generation in PC12 cells . The effect of Prx-I on PC12 cells was potentiated in the presence of mena dione, and suppressed by an inhibitor of nitric oxide synthetase. Prx-II tr ansduction resulted in 25-35% lower levels of glutathione (GSH) in both cel l types, while Prx-I transduction increased GSH levels in neurons and decre ased GSH and caspase-3 activity in fibroblasts. Prx-I and Prx-II also had d iffering effects on cell viability. These results suggest that Prx-I and Pr x-II can either increase or decrease intracellular oxidative stress dependi ng on cell type or experimental conditions, particularly conditions affecti ng nitric oxide levels.